27 - Chronic Kidney Disease

Question 1

What is done to identify chronic kidney disease in px w/ diabetes?

Answer 1

Screening for proteinuria & assessment of sCr converted into eGFR

Question 2

All px w/ CKD considered high risk for _____

Answer 2

CV events

Question 3

How can progression of CKD in diabetes be slowed?

Answer 3

Use of medications that disrupt RAAS

Question 4

Earliest stage of diabetic nephropathy = ____

Answer 4

Hyperfiltration (GFR significantly higher than normal)

Question 5

Earliest clinical sign of diabetic nephropathy is _____

Answer 5

Persistent albuminuria

Question 6

What should be done for prevention of diabetic nephropathy?

Answer 6

• Optimal glycemic control ASAP after diagnosis will reduce risk of developing diabetic kidney disease
• Optimal BP control
• Blockade of RAAS w/ ACEi or ARB can reduce risk of developing CKD independent of their effect on BP (protective effect demonstrated in px w/ diabetes & HTN, but not normotensive px w/ diabetes)

Question 7

What does albumin/creatinine ratio (ACR) describe?

Answer 7

• How much protein is in the urine and if there is renal dysfunction
• Need the ratio b/c don’t know if urine is dilute (drinking lots of water) or concentrated
• Creatinine shows how concentrated urine is

Question 8

What do the values of ACR mean?

Answer 8

• ACR 2-20 = microalbuminuria

- ACR 20-66.7 = over nephropathy (macroalbuminuria)

Question 9

What are some potential causes of transient albuminuria?

Answer 9

• Recent major exercise
• UTI
• Febrile illness
• Decompensated CHF
• Menstruation
• Acute severe elevation in blood glucose or BP

Question 10

How can you decrease albuminuria?

Answer 10

Decrease amount of pressure on glomerulus

Question 11

Which drug should be given to adults w/ diabetes & CKD w/ either HTN or albuminuria? What should be monitored?

Answer 11

• ACE inhibitor/ ARB and started at very low dose to slow progression of diabetic nephropathy
• Check sCr and K+ in first 2 weeks
• ACEi or ARB can cause dramatic increase in sCr in short period of time; this is caused by renal artery stenosis or on a sick day
• ACE inhibitor in type 1 w/ macroalbuminuria reduces renal outcomes
• Don’t use ACE & ARB together b/c increased risk of AKI & hyperkalemia

Question 12

How long can ACEi or ARBs be safely continued in px w/ declining renal function over time?

Answer 12

Based on Lexicomp

• ACE inhibitors require dosage changes for renal dysfunction (decreased dose or frequency < 30 mL/min)
• ARBs don’t require dosage changes

Question 13

What normally accompanies hyperphosphatemia?

Answer 13

Hypocalcemia and low serum levels of vitamin D

Question 14

When are oral phosphate binders used?

Answer 14

Majority (over 90%) of px w/ kidney failure b/c dietary restriction isn’t enough to control hyperphosphatemia

Question 15

Renagel - MOA, dose, SE, advantage, disadvantage

Answer 15

• Binds to phosphate w/o calcium (polysaccharide complex) so doesn’t cause hypercalcemia
• Usually 800 mg TID w/ meals
• GI effects (N/V, abdominal pain, bloating, diarrhea), hypercalcemia, metabolic acidosis
• Advantage = effective & doesn’t contain calcium & reduces LDL
• Disadvantage = GI effects & higher cost

Question 16

Calcium carbonate - SE, advantage, disadvantage

Answer 16

• Interferes w/ absorption of aspirin, digoxin, isoniazid, quinolone, tetracycline
• AE = GI effects (N/V, diarrhea, constipation), hypercalcemia, xerostomia
• Advantage = effective & inexpensive
• Disadvantage = may contribute to hypercalcemia, promote vascular calcification, or both

Question 17

What is the target phosphate serum level?

Answer 17

1.8 mmol/L

Question 18

What is the relationship between the kidneys and vitamin D?

Answer 18

Kidneys are the final activation of vitamin D in the body, so when kidneys aren’t working then vitamin D doesn’t get activated

Question 19

What is calcitriol?

Answer 19

• Activated vitamin D

- Has inhibitory effect on parathyroid gland

Question 20

Which px can’t receive calcitriol?

Answer 20

Px w/ hypercalcemia (> 2.6) or hyperphosphatemia (> 1.8) b/c calcitriol will make phosphate & calcium higher (must control phosphates first)

Question 21

What happens to phosphate in end stage renal disease?

Answer 21

Phosphate builds up in blood b/c can’t be filtered out by kidneys

Question 22

What is the relationship between calcium and phosphate? Is this good?

Answer 22

Calcium & phosphate bind together, but don’t want calcium-phosphate to stay around in the body b/c will calcify in the arteries (called calcium phosphate deposition); also deposits in subcutaneous fat under skin (causes you to become very itchy; this can break the skin & cause infection)

Question 23

Why don’t you want phosphate to be increased?

Answer 23

• Will bind to calcium and deposit in heart or subcutaneous fat
• Increased phosphate stimulates parathyroid gland (controls calcium levels) to release PTH (parathyroid hormone) that goes looking for calcium that needs to be replaced b/c phosphate is binding it all
• • Will go to the bones to find the calcium => can lead to osteitis fibrosa cystica

Question 24

How can phosphate be decreased?

Answer 24

Remove intake (processed meats, dairy products, can of soda)

Question 25

Where do phosphate and calcium normally bind and where do we want them to bind?

Answer 25

• Normally phosphate & calcium bind in the blood

- Want it to happen in stomach so you can poop them out (that’s why you give calcium supplementation w/ meals)

Question 26

What is the goal for PTH levels?

Answer 26

PTH (parathyroid hormone) should be < 200 ng/L in adults w/ chronic kidney disease (don’t know the exact amount for best protection)

Question 27

What causes renal osteodystrophy? What is the tx?

Answer 27

• Caused by hyperphosphatemia b/c too much phosphate binds all the calcium, so body takes calcium from bones
• Tx would be treatment of high phosphate, which is phosphate binders (ex: Renagel)